Search PubMed⌕ Search

Biomedical subjects

Ann E Perry

Publications and source records attributed to Ann E Perry.

11 recordsLinked to original sources
PubMed2007

Measures of cumulative exposure from a standardized sun exposure history questionnaire: a comparison with histologic assessment of solar skin damage.

Ultraviolet radiation exposure is the dominant environmental determinant of all major forms of skin cancer; however, the nature of the association is incompletely understood. Existing instruments to capture sun exposure history tend to yield reproducible results, but the validity of these responses is unknown. To address this question, the authors examined the relation between responses to a standardized sun exposure instrument and histologic evidence of actinic damage in a population-based study of keratinocyte cancers from New Hampshire diagnosed from July 1, 1997, through March 31, 2000. A single study dermatopathologist histologically reviewed the adjacent skin of 925 skin cancer biopsies for the presence of solar keratoses and the extent of solar elastosis. The authors compared these measures with responses to a personal interview on history of sunburns, sunbathing, and time spent outdoors. Focusing on site-specific exposure, they found variables that estimated cumulative exposure related to histologic evidence of actinic damage. In contrast, measures of acute/intermittent exposure were generally unrelated to solar damage histologically. Findings suggest that cumulative, but not intermittent, measures of sun exposure derived from a personal interview appear to reflect a person's exposure history based on histologic evidence.

Aged↗
PubMed2007

Factors associated with atypical moles in New Hampshire, USA.

Only a few studies, conducted in Sweden, assessed factors associated with the presence of atypical moles in the general population. We conducted a population-based, case-control study in New Hampshire, USA, to identify factors associated with atypical moles. In our study, atypical moles affected 14% of the study population. The adjusted odds ratio (OR) was 0.34 (95% confidence interval (CI) = 0.14-0.80) for those with the highest adulthood recreational sun exposure, relative to the lowest. The OR for any freckles, compared to none, was 2.24 (95% CI = 1.18-4.25). We found a linear relationship between the number of benign moles and the presence of atypical moles (p for trend = 0.0001). The OR was 7.34 (95% CI = 3.03-17.80) for > 15 benign moles, relative to 0-4. Our data indicate that freckles and benign moles, which may reflect melanocytic inducibility, are strongly associated with atypical moles. The inverse association with sun exposure should be considered with caution.

Adult↗
PubMed2006

Multiple primary melanoma: two-year results from a population-based study.

OBJECTIVE: To assess the frequency of occurrence and risk factors for multiple primary melanoma. DESIGN: Population-based, case-control study. SETTING: New Hampshire. PARTICIPANTS: Three-hundred fifty-four New Hampshire residents with a confirmed first diagnosis of cutaneous melanoma. MAIN OUTCOME MEASURE: Diagnosis of a subsequent primary cutaneous melanoma. RESULTS: An additional melanoma occurred in 27 individuals (8%) within 2 years of their initial diagnosis, including 20 (6%) within the first postdiagnosis year. In 9 (33%) of these 27 cases, at least 1 subsequent melanoma was deeper than the first tumor. The 27 individuals with a subsequent melanoma diagnosis were classified as "cases" and were compared on the basis of risk factors to the 327 "controls" with a single melanoma diagnosis. The data indicate an inverse relation of risk of multiple primary melanomas with multiple blistering sunburns (P = .01 for the trend); the odds ratio (OR) was 0.32 (95% confidence interval [CI], 0.11-0.93) for 2 or more sunburns compared with none. The number of atypical moles was significantly related to increased risk (P = .004 for the trend). The presence of 3 or more atypical moles compared with none was associated with more than a 4-fold risk of multiple primary melanomas (OR, 4.29; 95% CI, 1.51-12.16). CONCLUSIONS: Additional melanomas occur more frequently than previously shown. Our study confirms that atypical moles are strongly associated with risk of multiple primary melanomas but provides little evidence that risk is influenced by pigmentary characteristics, hours of sun exposure, or benign moles. The inverse association with blistering sunburn may reflect the influence of an unmeasured covariate.

Adult↗
PubMed2006

Allelic loss at Drosophila patched gene is highly prevalent in Basal and squamous cell carcinomas of the skin.

The human homolog of the Drosophila Patched gene (PTCH), located at chromosome 9q22.3, is frequently altered in both nevoid basal cell carcinoma syndrome, and sporadic basal cell carcinomas (BCCs). However, alteration of the PTCH gene locus has been poorly studied in squamous cell carcinoma (SCC). We analyzed loss of heterozygosity (LOH) at five markers in and around the PTCH gene in 276 keratinocyte tumors from a population-based study in New Hampshire. We found a high prevalence of any 9q22.3 LOH in both BCC (75.5%) and SCC (60.8%), with BCC being significantly more likely to have LOH than SCC (P<0.009). The PTCH gene was specifically lost in 60% of BCC, and 50% of SCC tumors. Among SCC tumors, 9q22 LOH was significantly more likely to occur in those who tend to burn (P<0.05), and this association was strongest for tumors that occurred on sun-exposed areas of the body (P<0.04). Additionally, 9q22 LOH occurred more frequently in SCC tumors associated with a history of severe sunburns (P<0.08). Thus, in our large, population-based sample, 9q22 loss, including PTCH, was highly prevalent in both BCC and SCC. Overall, these data support the hypothesis that PTCH loss is a common, early lesion for SCC and BCC.

Adult↗
PubMed2005

Pigmentary characteristics and moles in relation to melanoma risk.

Although benign and atypical moles are considered key melanoma risk factors, previous studies of their influence were small and/or institution-based. We conducted a population-based case-control study in the state of New Hampshire. Individuals of ages 20-69 with an incident diagnosis of first primary cutaneous melanoma were ascertained through the New Hampshire State Cancer Registry. Controls were identified through New Hampshire driver's license lists and frequency-matched by age and gender to cases. We interviewed 423 eligible cases and 678 eligible controls. Host characteristics, including mole counts, were evaluated using logistic regression analyses. Our results showed that pigmentary factors, including eye color (OR = 1.57 for blue eyes compared to brown), hair color (OR = 1.85 for blonde/red hair color compared to brown/black), freckles before age 15 (OR = 2.39 for freckles present compared to absent) and sun sensitivity (OR = 2.25 for peeling sunburn followed by no tan or a light tan and 2.42 for sunburn followed by tan compared to tanning immediately), were related to melanoma risk; these associations held after adjustment for sun-related factors and for moles. In analyses confined to skin examination participants, the covariate-adjusted effects of benign and atypical moles were moderately strong. Compared to 0-4 benign moles, risk increased steadily for 5-14 moles (OR = 1.71), 15-24 moles (OR = 3.55) and >or= 25 moles (OR = 4.33). Risk also increased with the number of atypical moles; compared to none, the ORs for having 1, 2-3, or >or= 4 atypical moles were 2.08, 1.84 and 3.80, respectively. Although risk was highest for those with multiple benign and atypical moles, the interaction was not of statistical significance. Our findings, arising from the first population- and incidence-based study to evaluate atypical moles in relation to melanoma risk, confirm the importance of host susceptibility, represented by pigmentary factors and the tendency to develop benign or atypical moles, in the etiology of this disease.

Adult↗
PubMed2002

Microsatellite instability at tetranucleotide repeats in skin and bladder cancer.

Recently, a novel form of MSI has been described that occurs only at tetranucleotide repeat markers. This has been termed elevated microsatellite instability at selected tetranucleotide repeats (EMAST). EMAST has been related to alterations of the p53 gene, and to the nature of the repeat sequence. We initially tested whether loss of heterozygosity (LOH) at the p53 and the patched (ptch) genes was related to EMAST in a series of 61 non-melanoma skin cancer (NMSC) tumors. We then analysed a series of 57 primary bladder cancers for the presence of EMAST, testing whether this was related to mutation or expression of the p53 gene. In both NMSC and bladder tumors we found a high prevalence of EMAST (75.4 and 43.9%). In NMSC the prevalence of EMAST was higher in tumors that had either p53 or ptch LOH, although the difference was not statistically significant. There was a significant association of extensive EMAST (three or more loci) with mutations in p53 among the bladder cancer tumors, but no indication of elevated EMAST in tumors with abnormal p53 staining without mutation. The association of EMAST with p53 mutation was confined to non-invasive disease. Hence, EMAST likely reflects a particular pattern of somatic events that are interactive with p53 mutation, particularly common in skin cancer and limited to non-invasive disease in bladder cancer.

Female↗
PubMed2002

Alteration of chromosome 9p21 and/or p16 in benign and dysplastic nevi suggests a role in early melanoma progression (United States).

OBJECTIVE: The importance of p16 alterations in the pathogenesis of dysplastic nevi and sporadic melanoma remains controversial. The goal of this work was to discover if p16/9p21 alterations occur early in precursor lesions as well as related sporadic melanomas. METHODS: DNA was microdissected from 44 cutaneous melanomas, 14 dysplastic nevi, and six nevi without atypia as part of a study of melanoma. Alteration of the p16 region on 9p21 was measured by loss of heterozygosity (LOH) analysis as well as detection of homozygous deletions for p16 exon 2. RESULTS: This analysis revealed that LOH in 9p21 directly surrounding p16 occurred in approximately 40% (17/44) of melanoma tumors representing all Clark levels. LOH was also discovered in 64% (9/14) of dysplastic nevi, and 50% (3/6) of benign nevi. Homozygous deletion of p16 was found in 29% (4/14) of dysplastic nevi but never in benign nevi. CONCLUSIONS: These studies reveal that LOH and homozygous deletion can affect 9p21 and the p16 locus early in putative precursor lesions of melanoma, even prior to the establishment of cytologically evident aberrant histology. Comparison of alterations in nevi and melanomas from the same individual revealed a pattern of progressive but heterogeneous events suggesting that systemic processes may affect this region of 9p21 at various times during melanoma progression.

Adult↗
PubMed2002

Type-I cryoglobulinemia-like histopathologic changes in tick bites: a useful clue for tissue diagnosis in the absence of tick parts.

BACKGROUND: The histopathologic findings of localized reactions to tick bites may present as diagnostic dilemmas, especially if there is no history of a tick bite, or if the tick's mouthparts are not present in the biopsied skin. OBJECTIVE: Skin biopsies of patients with a clinical history of a tick bite were selected and reviewed with the aim of detecting a common histopathologic denominator which could serve as a useful clue to the diagnosis, especially when the tick's mouthparts are absent. METHODS: Hematoxylin and eosin-stained slides of 15 skin biopsies of tick bites were retrieved from three dermatopathology and pathology laboratories. Where additional paraffin-embedded tissue was available, additional sections were also stained with periodic acid-Schiff (PAS) and phosphotungstic acid-hematoxylin (PTAH). RESULTS: In every case in which adequate tissue was available (13/ 15 biopsies), the capillaries and postcapillary venules of the superficial and deep vascular plexi adjacent to the attachment's site were filled with thrombi. Fibrin thrombi were seen in association with other more numerous thrombi characterized by homogeneous eosinophilic hyaline material similar to the cryoprecipitate present in type I (monoclonal) cryoglobulinemia. All thrombi were positive for PAS and PTAH; however, the latter staining was minimally present in the hyaline thrombi. In most cases, the site of the tick bite showed ulceration, with an underlying wedge-shaped superficial and deep perivascular and occasionally interstitial mixed lymphohistiocytic infiltrate. In addition, there were eosinophils, numerous neutrophils and extravasated erythrocytes. Other findings included suppurative necrosis (7/15) cases, giant-cell reaction (one case), fat necrosis (one case) and eccrine gland necrosis (one case). CONCLUSIONS: Vascular eosinophilic hyaline thrombi were found to be a frequent histologic manifestation of a tick bite. This finding may be related to the secretory products of the tick's saliva during inoculation. We believe that a tick bite should be suspected when focal intravascular hyaline occlusion is observed, and that it should be included in the differential diagnosis of type I (monoclonal) cryoglobulinemia, even if there is no history of a tick bite or if tick parts are not present in the skin biopsy specimen.

Adult↗
PubMed2002

Sebaceous carcinoma in children.

Sebaceous carcinoma is a rare malignant tumor derived from the epithelium of sebaceous glands. It potentially may develop from any sebaceous gland, but most commonly occurs in the periorbital area. We report a case of sebaceous carcinoma in a 14-year-old girl who was first seen with an asymptomatic 2.5 x 2.3-cm firm, multilobulated cutaneous nodule on the anterior thorax, which had been present for 1 year. She was adopted, and no family history is available. A skin biopsy specimen revealed a poorly differentiated infiltrative carcinoma involving the dermis and subcutaneous fat and focally involving the epidermis. Tumor cells had sebaceous and squamous differentiation. A diagnosis of sebaceous carcinoma was made. She was treated by surgical excision with a 2-cm margin. Further work-up showed no evidence of Muir-Torre syndrome.

Adenocarcinoma, Sebaceous↗